Open-angle glaucoma (OAG) afflicts 2% of the population over 40 years of age. Its etiology and the factors responsible for its progression are unknown. The ultimate objective of this project is to determine the mechanisms responsible for the malfunction of the aqueous outflow pathways in glaucoma. Our hypothesis is that major tissue alterations afflict the trabecular meshwork in Primary Open-Angle Glaucoma. We will examine glucoma specimens and compare them with age-matched normals using new quntitative as well as qualitataive methods. Our hypothesis will be further tested by analysing connective tissues changes in the outflow pathways of secondary open-angle glaucoma and in experimental studies to better define the relationship of cell loss and connective tissue change.